DNC News

Vitamin D and Co Q-10 both show promise in treating Congestive Heart Failure

Jacob Schor, ND

April 21, 2006


Vitamin D:

Vitamin D research has taken a turn. For the last half dozen years research on vitamin D has focused on linking deficiency with development of morbidity. Links between low vitamin D status and a variety of disease have been demonstrated ranging from auto immune diseases such as rheumatoid arthritis, diabetes and multiple sclerosis to cancer.


The focus of research is shifting. Now researchers have begun to ask whether vitamin D supplementation can change the course of these diseases.


A paper appeared in this month's edition of the American Journal of Clinical Nutrition reporting on the effect of vitamin D on patients with Congestive Heart Failure (CHF).


German researchers gave 2,000 IU/day of vitamin D in a randomized, placebo-controlled study involving 123 subjects with congestive heart failure (CHF). Subjects were divided into two groups. Group 1 received vitamin D and calcium (500 mg/day), while Group 2 (control group) received a placebo and calcium. 93 patients completed the study. Group 1, the vitamin D people, had a 43% increase in interleukin-10 (IL-10), an anti-inflammatory cytokine, and a significant decrease in parathyroid hormone. Subjects in Group 2, the placebo group, had a 12% increase in, tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine, while the vitamin D group did not. These pro-inflammatory cytokines may contribute to development of CHF. There was no statistically significant difference in survival dat 15 months. Even so the fact that vitamin D could reduce inflammation in patients with CHF lead the authors to suggest CHF patients could benefit from 2,000 IU of vitamin D per day. [i]


Back in 1997 an article in the American Journal of Medicine reported that people with CHF had surprisingly low vitamin D levels. About half of people with severe CHF had osteopenia or osteoporosis. Markers of bone turnover were frequently abnormal and were more so with more severe disease. [ii] A report a few years later linked low vitamin D and resulting high parathyroid hormones with CHF. [iii] These studies are not surprising as the epidemiological link between sun exposure on heart disease risk is well established.


What is new is the attempt to measure benefit in treating CHF with vitamin D supplementation. Just because deficiency causes or is associated with a disease, it does not necessarily follow that supplementations will cure the disease. Although we wouldn't complain even if it just helped treat it. Expect to see results of other intervention trials with Vitamin D being supplemented in diseases which have been linked to deficiency.


Coenzyme Q-10

While on the subject of congestive heart failure another interesting study showed up last November in the European Heart Journal, this one using a multivitamin plus Coenzyme Q-10 at 150 mg/day. The multivitamin/mineral supplement contained high levels of vitamins B 1 and B 6 (200 mg each), folic acid (5000 mcg), B 12 (200 mcg), vitamin C (500 mg), vitamin E (400 IU). In the placebo group the disease continued to progress: left ventricular volumes increased 4% in the placebo group but decreased 13% in the supplemented group. Left ventricular ejection fraction remained essentially unchanged in the placebo group while improving 21% in the supplemented group. Quality-of-life scores improved 9.5% in the supplemented group while declining 1% in the placebo group. [iv]


These results are interesting if just a little confusing to practitioners. Earlier trials have shown that CoQ10 improves heart function in CHF patients. Unfortunately, in the current study there is no way to separate the effect of the Co Q-10 from that of the vitamins. We don't know whether the effect came from the Co Q-10 alone or the multivitamins increased the benefit further. For the time being adding multivitamins in addition to Co Q-10 should be done on the basis of the, “can't hurt and might help” principle.




Am J Clin Nutr. 2006 Apr;83(4):754-9.

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Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial.

Schleithoff SS , Zittermann A , Tenderich G , Berthold HK , Stehle P , Koerfer R .

Institute of Nutrition and Food Science, University of Bonn , Bonn , Germany .

BACKGROUND: Elevated circulating concentrations of proinflammatory cytokines may contribute to the pathogenesis of congestive heart failure (CHF). In vitro studies suggest that vitamin D suppresses proinflammatory cytokines and increases antiinflammatory cytokines. OBJECTIVE: We evaluated the effect of vitamin D supplementation on the survival rate and different biochemical variables in patients with CHF. DESIGN: One hundred twenty-three patients randomly received either 50 mug vitamin D(3)/d plus 500 mg Ca/d [D(+) group] or placebo plus 500 mg Ca/d [D(-) group] for 9 mo. Biochemical variables were assessed at baseline and after 9 mo. The survival rate was calculated for a follow-up period of 15 mo. RESULTS: Ninety-three patients completed the study. Significant treatment effects were observed on logarithmic-transformed serum concentrations of 25-hydroxyvitamin D (P = 0.001), parathyroid hormone (P = 0.007), tumor necrosis factor alpha (P = 0.006), and interleukin 10 (P = 0.042). 25-Hydroxyvitamin D increased by 26.8 ng/mL in the D(+) group but increased only by 3.6 ng/mL in the D(-) group. Compared with baseline, parathyroid hormone was significantly lower and the antiinflammatory cytokine interleukin 10 was significantly higher in the D(+) group after 9 mo. The proinflammatory cytokine tumor necrosis factor alpha increased in the D(-) group but remained constant in the D(+) group. The survival rate did not differ significantly between the study groups during the follow-up period. CONCLUSIONS: Vitamin D(3) reduces the inflammatory milieu in CHF patients and might serve as a new antiinflammatory agent for the future treatment of the disease. Our data provide evidence for the involvement of an impaired vitamin D-parathyroid hormone axis in the progression of CHF.

PMID: 16600924 [PubMed - in process]



Am J Med. 1997 Sep;103(3):197-207.

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Comment in:

•  Am J Med. 1998 May;104(5):508-9.

•  Am J Med. 1998 Oct;105(4):358.

•  Am J Med. 1998 Oct;105(4):358-9.

•  Am J Med. 1999 Jul;107(1):102-3.

Bone mass, vitamin D deficiency, and hyperparathyroidism in congestive heart failure.

Shane E , Mancini D , Aaronson K , Silverberg SJ , Seibel MJ , Addesso V , McMahon DJ .

Department of Medicine, College of Physicians and Surgeons, Columbia University, New York , New York 10032 , USA .

PURPOSE: In contrast to renal and hepatic failure, congestive heart failure (CHF) has not been associated with a defined metabolic bone disorder. However, low bone mass has been reported in patients with CHF who receive a cardiac transplant. Both the pathophysiology and therapy of CHF may influence bone and mineral homeostasis and evidence that calciotropic hormones may affect cardiovascular function is accumulating. Therefore, we evaluated patients with severe CHF to determine the prevalence of osteoporosis and to characterize relationships between mineral homeostasis, bone turnover, bone mass, and severity of CHF. PATIENTS AND METHODS: One hundred one patients (79 men and 22 women, aged 25 to 70 years) with severe CHF (New York Heart Association functional class III or IV) referred for consideration for cardiac transplantation were evaluated with measurements of serum 25-hydroxyvitamin D (25-OHD), 1,25 dihydroxyvitamin D [1,25(OH)2D], intact parathyroid hormone (PTH), markers of bone turnover (serum osteocalcin, urinary hydroxyproline, and pyridinium crosslinks); bone mineral density (BMD) by dual energy x-ray absorptiometry was measured in 91 patients. Left ventricular ejection fraction (LVEF) and resting cardiac output (CO) were determined in 88 and maximal treadmill exercise testing and peak oxygen consumption were performed in 45 patients. RESULTS: Osteoporosis (T score < or = -2.5) was present in 7% at the lumbar spine, 6% at the total hip, and 19% at the femoral neck. Osteopenia (T scores between -1.0 and -2.5) was present in 43% at the lumbar spine, 47% at the total hip, and 42% at the femoral neck. Women were more severely affected (P = 0.007). Frankly low serum 25-OHD (< or = 9 pg/mL) and 1,25(OH)2D (< or = 15 pg/mL) levels were found in 17% and 26% of the patients, respectively, and elevated serum PTH (> or = 65 pg/mL) in 30%. Both low serum 1,25(OH)2D and increased serum PTH were associated with prerenal azotemia. Low serum vitamin D metabolites were associated with biochemical evidence of increased bone turnover, but BMD did not differ by vitamin D or PTH status. Patients with more severe CHF had significantly lower vitamin D metabolites and higher bone turnover, whereas elevated PTH was associated with better LVEF (21 +/- 1 versus 18 +/- 1%; P = 0.05) and correlated positively with resting CO (R = 0.220; P = 0.04). CONCLUSIONS: Osteopenia or osteoporosis were observed in approximately half of these patients with severe CHF. Abnormal calciotropic hormone concentrations, also common, were associated with evidence of increased bone resorption but were not related to BMD in this cross-sectional study. Abnormal concentrations of calciotropic hormones were related to the severity of cardiovascular compromise. Because both low BMD and low serum concentrations of 25-OHD in patients with CHF are associated with higher rates of bone loss and fracture after cardiac transplantation, patients should be evaluated for and receive appropriate therapy for these disorders.

PMID: 9316552 [PubMed - indexed for MEDLINE]



J Am Coll Cardiol. 2003 Jan 1;41(1):105-12.

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Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure?

Zittermann A , Schleithoff SS , Tenderich G , Berthold HK , Korfer R , Stehle P .

Department of Nutrition Science, University of Bonn , Germany . a.zittermann@uni-bonn.de

OBJECTIVES: This study was designed to evaluate the association between vitamin D status and congestive heart failure (CHF). BACKGROUND: Impaired intracellular calcium metabolism is an important factor in the pathogenesis of CHF. The etiology of CHF, however, is not well understood. METHODS: Twenty patients age <50 years and 34 patients age >/=50 years with New York Heart Association classes >/=2 and 34 control subjects age >/=50 years were recruited. N-terminal pro-atrial natriuretic peptide (NT-proANP), a predictor of CHF severity; vitamin D metabolites; and parameters of calcium metabolism were measured in fasting blood samples collected between November 2000 and March 2001. RESULTS: Both groups of CHF patients had markedly increased serum levels of NT-proANP (p < 0.001), increased serum phosphorus levels (p < 0.001), and reduced circulating levels of both 25-hydroxyvitamin D (p < 0.001) and calcitriol (p < 0.001). Albumin-corrected calcium levels were reduced and parathyroid hormone levels were increased in the younger CHF patients compared with the controls (both p values <0.001). Moreover, parathyroid hormone levels tended to be higher in the elderly CHF patients than in the controls (p = 0.074). In a nonlinear regression analysis 25-hydroxyvitamin D and calcitriol were inversely correlated with NT-proANP (r(2) = 0.16; p < 0.001 and r(2) = 0.12; p < 0.01, respectively). The vitamin D genotype at the BmsI restriction site did not differ between the study groups. CONCLUSIONS: The low vitamin D status can explain alterations in mineral metabolism as well as myocardial dysfunction in the CHF patients, and it may therefore be a contributing factor in the pathogenesis of CHF.

PMID: 12570952 [PubMed - indexed for MEDLINE]




Eur Heart J. 2005 Nov;26(21):2238-44. Epub 2005 Aug 4.

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The effect of micronutrient supplementation on quality-of-life and left ventricular function in elderly patients with chronic heart failure.

Witte KK , Nikitin NP , Parker AC , von Haehling S , Volk HD , Anker SD , Clark AL , Cleland JG .

Department of Academic Cardiology, Castle Hill Hospital , Castle Road , Cottingham, Hull HU16 5JQ , UK . klauswitte@hotmail.com

AIMS: Chronic heart failure (CHF) is a common and leading cause of death in industrialized countries. The potential benefits of micronutrient supplementation in CHF are extensive. Therefore, we examined the influence of long-term multiple micronutrient supplementation on left ventricular ( LV ) function, levels of pro-inflammatory cytokines, and quality-of-life (QoL) in elderly patients with CHF. METHODS AND RESULTS: Thirty CHF patients [age 75.4 (0.7), mean (SEM), LV ejection fraction (LVEF) < or =35%] were randomized to receive capsules containing a combination of high-dose micronutrients (calcium, magnesium, zinc, copper, selenium, vitamin A, thiamine, riboflavin, vitamin B(6), folate, vitamin B(12), vitamin C, vitamin E, vitamin D, and Coenzyme Q10) or placebo for 9 months in a double-blind fashion. All subjects were on stable optimal medical therapy for at least 3 months before enrolment. At randomization and at study end, tumour necrosis factor-alpha and its soluble receptors TNFR-1 and TNFR-2 were measured and six-minute walk test and QoL were assessed. Cardiac magnetic resonance scanning was performed to evaluate cardiac dimensions and LVEF. Two patients died during follow-up. The remaining patients (14 randomized to placebo and 14 to micronutrients) were well matched for LV function, symptoms, and exercise capacity. At the end of the follow-up period, LV volumes were reduced in the intervention group with no change in the placebo group [-13.1 (17.1)% vs. +3.8 (10.0)%; P<0.05]. LVEF increased by 5.3+/-1.4% in the intervention group and was unchanged in the placebo group (P<0.05). Patients taking micronutrients also had a significant improvement in QoL score between enrolment and study end [+9.5 (1.6)%; P<0.05], whereas those taking placebo had a slight deterioration [-1.1 (0.8)%; P=0.12]. Six-minute walk test and inflammatory cytokine levels remained unchanged in both groups. CONCLUSION: Long-term multiple micronutrient supplementation can improve LV volumes and LVEF and QoL scores in elderly patients with heart failure due to LV systolic dysfunction.




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